推荐产品
方案
≥98.0% (TLC)
表单
powder
脂质类型
sphingolipids
储存温度
−20°C
SMILES字符串
OC[C@@](N)([H])[C@]([H])(O)/C=C/CCCCCCCCCCCCC
InChI
1S/C18H37NO2/c1-2-3-4-5-6-7-8-9-10-11-12-13-14-15-18(21)17(19)16-20/h14-15,17-18,20-21H,2-13,16,19H2,1H3/b15-14+/t17-,18+/m0/s1
InChI key
WWUZIQQURGPMPG-KRWOKUGFSA-N
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生化/生理作用
细胞膜的一种组成部分。神经酰胺的前体。蛋白激酶 C 的选择性抑制剂，但不抑制蛋白激酶 A 或肌球蛋白轻链激酶。钙调蛋白依赖性酶的抑制剂。
包装
无底玻璃瓶。内含物在插入的融合锥体内。
危险声明
预防措施声明
危险分类
Aquatic Chronic 4
储存分类代码
11 - Combustible Solids
WGK
WGK 3
闪点(°F)
Not applicable
闪点(°C)
Not applicable
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Neurology, 81(2), 174-181 (2013-05-24)
To study the immune response against varicella-zoster virus (VZV) in patients with multiple sclerosis before and during fingolimod therapy. The VZV-specific immune response was studied using interferon (IFN)-γ enzyme-linked immunosorbent spot assay, proliferation assays, and upregulation of T-cell activation markers
Mei-Hong Li et al.
Pediatric blood & cancer, 60(9), 1418-1423 (2013-05-25)
Neuroblastoma (NB) is the most common extra-cranial solid tumor in childhood. Poor outcomes for children with advanced disease underscore the need for novel therapeutic strategies. FTY720, an immunomodulating drug approved for multiple sclerosis, has been investigated in oncology with promising
Vilija G Jokubaitis et al.
Neurology, 82(14), 1204-1211 (2014-03-13)
To determine early risk of relapse after switch from natalizumab to fingolimod; to compare the switch experience to that in patients switching from interferon-β/glatiramer acetate (IFN-β/GA) and those previously treatment naive; and to determine predictors of time to first relapse
David Henault et al.
Neurology, 81(20), 1768-1772 (2013-10-18)
To determine the range of fluctuation in total lymphocyte counts (TLCs) in peripheral blood over a 4- to 7-year period in patients with MS receiving fingolimod (FTY720) and the relation between TLCs and T-cell subsets (CD4+, CD8+, CCR7+/-) that are
Paolo Neviani et al.
The Journal of clinical investigation, 123(10), 4144-4157 (2013-09-04)
The success of tyrosine kinase inhibitors (TKIs) in treating chronic myeloid leukemia (CML) depends on the requirement for BCR-ABL1 kinase activity in CML progenitors. However, CML quiescent HSCs are TKI resistant and represent a BCR-ABL1 kinase-independent disease reservoir. Here we
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